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The anticancer ability of CHE is focused on cell apoptosis

This overall design gives the impression of an enzyme that was built by retrofitting a new C-terminal active site onto an existing NADPH-dependent reductase (Schmidt and Davies, 2007), either by classical exon shuffling (Margulies and McCluskey, 1985) or by mutation of the stop codon and translational read-through into previously 3-untranslated sequences (Novoselov and Gladyshev, 2003)

5.3.1 Fatty acid synthesis inhibitors (FASN/ACC inhibitors) Directly targeting the upregulated FAS pathway (e.g., FASN or ACC1) in pathogenic Th17 cells is a direct strategy to inhibit these cells (263)